1. Field of the Invention
The present invention relates to a pharmaceutical composition for treating acne. More particularly, the present invention relates to a therapeutic composition for treating acne, which includes eicosapentaenoic acid and .alpha.-linolenic acid.
2. Description of the Prior Art
Pharmaceutical compositions for treating acne generally include ointments containing synthetic chemicals, especially hormones, as an active ingredient, and are well known in the art. However, such prior art compositions suffer from a number of disadvantages such as, for example, (a) the application thereof results in greatly different skin reactions for every patient and, therefore, each composition must be carefully selected, (b) the compositions may cause severe allergic reactions and thus complicate the skin problems rather than treat the acne, and (c) when the treatment is discontinued, acne readily reoccurs.
The specific cause of acne is not yet clearly identified. It is only well known that the cause of inflammatory skin conditions such as acne, etc., is leukotrienes B.sub.4, C.sub.4, D.sub.4, E.sub.4 and the like, produced by the degradation of arachidonic acid, which is a constituent of phospholipids present in the skin endothelium. This is caused by the action of several enzymes such as, for example, 5-lipoxygenase, glutathione peroxidase, hydrolase, glutamyl transferase, glutamyl transpeptidase, dipeptidase, etc. In addition, it has been disclosed that the other cyclooxygenase enzymatic degradation products, i.e., prostaglandin E.sub.2 and thromboxane B.sub.2, may cause skin inflammation.
Furthermore, patients may produce skin-sensitive degradation products because of their health condition. Such degradation products may also act as one of the causes of skin acne or of the worsening of the acne condition. Among the above-mentioned causes, it is commonly and clearly recognized that arachidonic acid, as the primary degradation product of skin phospholipids, is decomposed to produce several degradation products which act as causes of acne.
Phospholipids present in the cell membrane of the facial skin tissue contain a great quantity of arachidonic acid. Arachidonic acid is converted into free arachidonic acid by the action of phospholipase A.sub.2 and then is metabolized by cyclooxygenase to produce 2-series prostaglandins, and then by lipoxygenase to produce 4-series leukotrienes. Among these metabolites, particularly prostaglandin E.sub.2, thromboxane B.sub.2, leukotrienes B.sub.4, C.sub.4, D.sub.4, E.sub.4 and the analogs thereof, may act as the cause of numerous inflammatory conditions in human body.
For example, Simmons et al (Biochemistry and Pharmacology, 1983) and Haworth et al (Inflammatory Mediators, 1985) have demonstrated that leukotriene B.sub.4 is present in large quantity in acute inflammatory tissue. In addition, Robinson et al (Prostaglandins, 1975) have reported that prostaglandin E.sub.2 is the cause of inflammatory conditions. Accordingly, extensive studies have been conducted to find a method for preventing the binding of arachidonic acid to cell membrane phospholipids and inhibiting the production of eicosanoids from arachidonic acid.
Thus, Yoe et al (Biochimica et Biophysica Acta, 1989a), who are also the inventors of the present invention, showed that a drastic reduction in the amount of arachidonic acid in cell membranes could be achieved by replacing arachidonic acid (an n-6 fatty acid) with eicosapentaenoic acid (EPA), which is an n-3 fatty acid. Also, Yeo et al have demonstrated the substitution effect of eicosapentaenoic acid for arachidonic acid by confirming that the biosynthesis of arachidonic acid significantly decreases while the biosynthesis of eicosapentaenoic acid and docosahexaenoic acid greatly increases from the examination of the synthesis of various fatty acids in experimental animals (Sprague-Dawley rats) to which eicosapentaenoic acid is administered and then (.sup.3 H) glycerol is injected.